Effect of straight-leg-raising movement on epidural fibrosis in early stage after laminectomy in a rabbit model

2006 ◽  
Vol 26 (6) ◽  
pp. 713-715
Author(s):  
Jijun Zhao ◽  
Shuhua Yang ◽  
Zhengwei Li ◽  
Yong Hu
Keyword(s):  
Early Stage ◽  
Rabbit Model ◽  
Epidural Fibrosis ◽  
Straight Leg Raising

Parathyroid hormone promotes cartilage healing after free reduction of mandibular condylar fractures by upregulating Sox9

2021 ◽  
pp. 153537022110271
Author(s):  
Yuanyuan Jia ◽  
Liuqin Xie ◽  
Zhenglong Tang ◽  
Dongxiang Wang ◽  
Yun Hu ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Internal Fixation ◽  
Early Stage ◽  
Rabbit Model ◽  
Mandibular Condyle ◽  
Fracture Site ◽  
Control Group ◽  
Condylar Cartilage ◽  
Cartilage Healing ◽  
Experimental Group

After high fractures of the mandibular condyle, the insufficient blood supply to the condyle often leads to poor bone and cartilage repair ability and poor clinical outcome. Parathyroid hormone (PTH) can promote the bone formation and mineralization of mandibular fracture, but its effects on cartilage healing after the free reduction and internal fixation of high fractures of the mandibular condyle are unknown. In this study, a rabbit model of free reduction and internal fixation of high fractures of the mandibular condyle was established, and the effects and mechanisms of PTH on condylar cartilage healing were explored. Forty-eight specific-pathogen-free (SPF) grade rabbits were randomly divided into two groups. In the experimental group, PTH was injected subcutaneously at 20 µg/kg (PTH (1–34)) every other day, and in the control group, PTH was replaced with 1 ml saline. The healing cartilages were assessed at postoperative days 7, 14, 21, and 28. Observation of gross specimens, hematoxylin eosin staining and Safranin O/fast green staining found that every-other-day subcutaneous injection of PTH at 20 µg/kg promoted healing of condylar cartilage and subchondral osteogenesis in the fracture site. Immunohistochemistry and polymerase chain reaction showed that PTH significantly upregulated the chondrogenic genes Sox9 and Col2a1 in the cartilage fracture site within 7–21 postoperative days in the experimental group than those in the control group, while it downregulated the cartilage inflammation gene matrix metalloproteinase-13 and chondrocyte terminal differentiation gene ColX. In summary, exogenous PTH can stimulate the formation of cartilage matrix by triggering Sox9 expression at the early stage of cartilage healing, and it provides a potential therapeutic protocol for high fractures of the mandibular condyle.

The prevention effect of poly (l-glutamic acid)/chitosan on spinal epidural fibrosis and peridural adhesion in the post-laminectomy rabbit model

2014 ◽  
Vol 23 (11) ◽  
pp. 2423-2431 ◽  
Author(s):  
Chunbo Li ◽  
Hong Wang ◽  
Haifei Liu ◽  
Jingbo Yin ◽  
Lei Cui ◽  
...  
Keyword(s):  
Glutamic Acid ◽  
Rabbit Model ◽  
Epidural Fibrosis ◽  
Spinal Epidural

scholarly journals Evidence of Ventricular Arrhythmogenicity and Cardiac Sympathetic Hyperinnervation in Early Cirrhotic Cardiomyopathy

2021 ◽  
Vol 12 ◽  
Author(s):  
Shin-Huei Liu ◽  
Li-Wei Lo ◽  
Yu-Hui Chou ◽  
Wei-Lun Lin ◽  
Tsung-Ying Tsai ◽  
...  
Keyword(s):  
Ventricular Arrhythmias ◽  
Sham Group ◽  
Early Stage ◽  
Sympathetic Innervation ◽  
Rabbit Model ◽  
Sympathetic Nerves ◽  
Structural Heterogeneity ◽  
Close Monitoring ◽  
Cirrhotic Cardiomyopathy ◽  
The Common

Cirrhotic cardiomyopathy (CMP) is associated with altered cardiac electrophysiological (EP) properties, which leads to the risk of ventricular arrhythmias (VAs). We aimed to evaluate the EP properties, autonomic, and structural remodeling in a rabbit model with early liver cirrhosis (LC). Twelve rabbits were assigned to the sham and LC groups. The early-stage LC was induced by the ligation of the common bile duct. All rabbits received an EP study, VA inducibility test, myocardial, and liver histology staining. Western blot analyses of protein expression and tyrosine hydroxylase stain for sympathetic nerves were performed. The effective refractory period the LC group was significantly longer than the sham group [i.e., left ventricle (LV) 205.56 ± 40.30 vs. 131.36 ± 7.94 ms; right ventricle (RV) 206.78 ± 33.07 vs. 136.79 ± 15.15 ms; left atrium (LA) 140.56 ± 28.75 vs. 67.71 ± 14.29 ms; and right atrium (RA) 133.78 ± 40.58 vs. 65.43 ± 19.49 ms, all p < 0.01], respectively. The VA inducibility was elevated in the LC group when compared with the sham group (i.e., 21.53 ± 7.71 vs. 7.76 ± 2.44%, p = 0.013). Sympathetic innervation (102/μm2/mm2) was increased in all cardiac chambers of the LC group compared with the sham group (i.e., LV 9.11 ± 4.86 vs. 0.17 ± 0.15, p < 0.01; RV 4.36 ± 4.95 vs. 0.18 ± 0.12, p = 0.026; LA 6.79 ± 1.02 vs. 0.44 ± 0.20, p = 0.018; and RA 15.18 ± 5.12 vs. 0.10 ± 0.07, p = 0.014), respectively. Early LC is presented with an increased ventricular vulnerability, structural heterogeneity, and sympathetic innervation. Close monitoring for fatal arrhythmias is warranted in patients with early stages of LC.

scholarly journals S-nitrosylation-mediated activation of a histidine kinase represses the type 3 secretion system and promotes virulence of an enteric pathogen

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Dan Gu ◽  
Yibei Zhang ◽  
Qiyao Wang ◽  
Xiaohui Zhou
Keyword(s):  
Histidine Kinase ◽  
Vibrio Parahaemolyticus ◽  
Early Stage ◽  
Rabbit Model ◽  
Secretion System ◽  
Intestinal Colonization ◽  
Type 3 Secretion System ◽  
Proinflammatory Factor ◽  
Type 3

AbstractVibrio parahaemolyticus is the leading cause of seafood-borne diarrheal diseases. Experimental overproduction of a type 3 secretion system (T3SS1) in this pathogen leads to decreased intestinal colonization, which suggests that T3SS1 repression is required for maximal virulence. However, the mechanisms by which T3SS1 is repressed in vivo are unclear. Here, we show that host-derived nitrite modifies the activity of a bacterial histidine kinase and mediates T3SS1 repression. More specifically, nitrite activates histidine kinase sensor VbrK through S-nitrosylation on cysteine 86, which results in downregulation of the entire T3SS1 operon through repression of its positive regulator exsC. Replacement of cysteine 86 with a serine (VbrK C86S mutant) leads to increased expression of inflammatory cytokines in infected Caco-2 cells. In an infant rabbit model of infection, the VbrK C86S mutant induces a stronger inflammatory response at the early stage of infection, and displays reduced intestinal colonization and virulence at the later stage of infection, in comparison with the parent strain. Our results indicate that the pathogen V. parahaemolyticus perceives nitrite as a host-derived signal and responds by downregulating a proinflammatory factor (T3SS1), thus enhancing intestinal colonization and virulence.

scholarly journals Upregulation of Myocardial and Vascular Phosphodiesterase 9A in A Model of Atherosclerotic Cardiovascular Disease

2018 ◽  
Vol 19 (10) ◽  
pp. 2882 ◽  
Author(s):  
Daniel Priksz ◽  
Mariann Bombicz ◽  
Balazs Varga ◽  
Andrea Kurucz ◽  
Rudolf Gesztelyi ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Vascular Function ◽  
Interstitial Fibrosis ◽  
Early Stage ◽  
Rabbit Model ◽  
Microvascular Dysfunction ◽  
Atherogenic Diet ◽  
Normal Diet ◽  
Guanosine Monophosphate ◽  
Atherosclerotic Cardiovascular Disease

Atherosclerosis is strongly associated with cardiac dysfunction and heart failure. Besides microvascular dysfunction and diminishment of the cardiac nitric oxide-Protein Kinase G (NO-PKG) pathway, recent evidence suggests that phosphodiesterase 9A (PDE9A) enzyme has an unfavorable role in pathological changes. Here, we characterized a rabbit model that shows cardiac dysfunction as a result of an atherogenic diet, and examined the myocardial PDE9A signaling. Rabbits were divided into Control (normal diet) and HC (atherogenic diet) groups. Cardiac function was evaluated by echocardiography. Vascular function was assessed, along with serum biomarkers. Histological stains were conducted, expression of selected proteins and cyclic guanosine monophosphate (cGMP) levels were determined. Signs of diastolic dysfunction were shown in HC animals, along with concentric hypertrophy and interstitial fibrosis. Endothelial function was diminished in HC rabbits, along with marked reduction in the aortic lumen, and increased left ventricle outflow tract (LVOT) pressures. A significant increase was shown in myocardial PDE9A levels in HC animals with unchanged vasodilator-stimulated phosphoprotein (VASP) phosphorylation and cGMP levels. Upregulation of PDE9A may be associated with early stage of cardiac dysfunction in atherosclerotic conditions. Since PDE9A is involved in cGMP degradation and in deactivation of the cardioprotective PKG signaling pathway, it may become an encouraging target for future investigations in atherosclerotic diseases.

scholarly journals Study On The Biomechanical Properties Of Rabbit Venous Arterialization

2019 ◽  
Author(s):  
Yuhao Zhang ◽  
Pei Niu ◽  
Zhimin Zhang ◽  
Xiaolong Niu ◽  
Wenzeng Shen ◽  
...  
Keyword(s):  
Early Stage ◽  
Artery Bypass ◽  
Rabbit Model ◽  
Biomechanical Properties ◽  
Arterial System ◽  
Nuclear Antigen ◽  
Minimal Damage ◽  
Alpha Actin ◽  
And Control ◽  
Proliferating Cell

Abstract Objective : To investigate the mechanisms underlying restenosis following coronary artery bypass grafting using bridging veins.Method : We established a rabbit model of venous arterialisation, by transplanting veins into the arterial system as bridging vessels and investigated vessel tensile mechanical and histomorphological properties. Result : Control vein elasticity (k = 16.20) was less than that of the control artery (k = 58.04; P < 0.05), and vein walls were thinner. Following venous arterialisation, proliferating cell nuclear antigen and alpha-actin were upregulated and vein walls thickened (P < 0.05), with elasticity after venous arterialisation (k = 86.26) significantly higher than that of control veins (P < 0.05). Conclusion : This indicates that venous intima is damaged by high pressure following arterialisation, resulting in gradual restenosis, with thickening of the venous intima and an increase in vessel elasticity. Clinically, there is potential to repeat these experiments to determine the elastic extremum of the great saphenous vein and control the pressure in the lumen of this vessel, to ensure minimal damage to the intima before anastomosis, thereby facilitating improvement of long-term patency rates following vein bridge surgery. Whether the increase in venous bridge elasticity after venous arterialisation can be controlled, with the aim of preventing early-stage restenosis, warrants investigation.

Utilization of longitudinal ultrasound measurements to quantify changes in knee joint synovial vascularity in a rabbit model of rheumatoid arthritis

2020 ◽  
Author(s):  
Hui Liu ◽  
Chao Huang ◽  
Shuqiang Chen ◽  
Qing Zheng ◽  
Yuhong Ye ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Time Course ◽  
Early Stage ◽  
Power Doppler ◽  
Rabbit Model ◽  
Knee Joints ◽  
Control Group ◽  
Vascular Morphology ◽  
Contrast Enhanced ◽  
Positive Correlations

Abstract Objective: This study of rabbits with ovalbumin-induced arthritis (OIA), a model of rheumatoid arthritis (RA), examined the time course of changes in synovial neovascularization based on imaging from power Doppler ultrasound (PDUS) and contrast-enhanced ultrasound (CEUS).Methods: 25 male New Zealand rabbits were in the OIA group and 5 were in the control group. Both rear knee joints of all rabbits were examined using conventional US and CEUS over 16 weeks. The knee synovia of OIA rabbits were sampled by US-guided biopsy, and the expression of CD31 and VEGF were determined by immunohistochemistry. The correlation of microvessel density (CD31 positivity) and VEGF at different times was analyzed using multimodal US.Results: OIA rabbits had increased synovial expression of CD31 and VEGF from week 6 to 12 (P<0.01). During the early stage of CEUS enhancement, dot enhancement was more common on weeks 6 and 8, and strip enhancement was more common on weeks 12 and 16 (P<0.05). There were significant positive correlations of synovial CD31 and VEGF expression with PDI grade, CEUS grade, and peak intensity (PI) (P<0.05 for all).Conclusions: OIA rabbits mimicked early-stage RA at 4 to 8 weeks, middle-stage RA at 8 to 12 weeks, and late-stage RA at 12 to 16 weeks. PDI, CEUS, and PI, especially when combined with CD31 expression, accurately characterized the extent of synovial vascularization. Increased vascular morphology based on CEUS may have value for the early diagnosis of RA.

scholarly journals ID: 1071 Establishing an early-stage femoral head necrosis model of rabbit using methylprednisolone and Complete Freund's Adjuvant

2017 ◽  
Vol 4 (S) ◽  
pp. 153
Author(s):  
Lan Thi Phi ◽  
Thuy Thi-Thanh Dao ◽  
Khanh Dinh-Van Nguyen ◽  
Phuc Van Pham ◽  
Khanh Hong-Thien Bui ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bone Marrow ◽  
Body Weight ◽  
Femoral Head ◽  
Early Stage ◽  
Rabbit Model ◽  
Femoral Head Necrosis ◽  
Group A ◽  
Freund's Adjuvant ◽  
Group B

Background: Pathological animal models provide the foundation for developing new methods for treating. This research aims to establish a rabbit model of femoral head necrosis. Osteonecrosis of the femoral head (ONFH) was induced in rabbits by using methylpresnisolone combined with Complete Freund's Adjuvant (CFA). New Zealand White rabbits were divided into two groups. Group A (n=10) was given an intramuscular injection of 0.5 mg/kg (CFA) and 40mg/kg methylprednisolone (MPS). Group B (n=6) was received normal saline at the same location and same volume as those in Group A. The efficiency of ONFH rabbit model was assessed at 7 weeks after the last injection. Body weight was weighed. The histological structure of head femoral and bone were deteded by H&E staining. The empty lacuna was counted. Cartilage degeneration was evaluated using image analysis software. Blood vessel density was assessed after ink artery infusion. The cell cycle of bone marrow-derived mononuclear cells was analyzed by flow cytometry. The results showed that there was no difference in body weight change of rabbits between two groups. However, the bone morphology and cartilage surface of femoral head were abnormalities at group A. The percentage of empty osteocyte lacunae were significantly higher in Group A than Group B. Chondrocyte degeneration and fibrocartilage expression were observed at Group A. Compare to group B, Group A had less ink-stained blood vessels. Moreover, the fraction of bone marrow-derived mononuclear at S phase and G2/M phase of the cell cycle was significantly decreased in group A. Thus, CFA combined with MPS can  be used to establishing an early-stage femoral head necrosis model of rabbit.

scholarly journals Development of an early-stage femoral head necrosis rabbit model using methylprednisolone and Complete Freund's Adjuvant

2017 ◽  
Vol 4 (11) ◽  
pp. 1749
Author(s):  
Lan Thi Phi ◽  
Ha Thi -Ngan Le ◽  
Thuy Thi -Thanh Dao ◽  
Khanh Dinh-Van Nguyen ◽  
Khanh Hong-Thien Bui ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bone Marrow ◽  
Body Weight ◽  
Femoral Head ◽  
Mononuclear Cells ◽  
Early Stage ◽  
Rabbit Model ◽  
Normal Group ◽  
Femoral Head Necrosis ◽  
Freund's Adjuvant

Introduction: Pathological animal models provide the foundation for developing new methods for disease treatment. This research aims to establish a rabbit model of femoral head necrosis. Methods: Osteonecrosis of the femoral head (ONFH) was induced in rabbits by using methylprednisolone (MPS) combined with Complete Freund's Adjuvant (CFA). New Zealand White rabbits were divided into two groups. ONFH group (n=10) was given an intramuscular injection of 0.5 mg/kg CFA and 40 mg/kg methylprednisolone. Normal group (n=6) received normal saline at the same location and same volume as those in ONFH group. The efficiency of the ONFH rabbit model was assessed at week 7 after the last injection. Body weight was detected, and the histological structure of head femoral and bone were assessed by H&E staining. The empty lacunae were counted. Cartilage degeneration was evaluated using image analysis software. Blood vessel density was assessed after ink artery infusion. The cell cycle of bone marrow-derived mononuclear cells was analyzed by flow cytometry. Results: The results showed that there was no difference in body weight changes of rabbits between the two groups. However, the bone morphology and cartilage surface of the femoral head showed abnormalities in the ONFH group. The percentage of empty osteocyte lacunae was significantly higher in ONFH group than normal group. Chondrocyte degeneration and fibrocartilage expression were observed in the ONFH group. Compared to the normal group, the ONFH group had less ink-stained blood vessels. However, the fraction of bone marrow-derived mononuclear cells in S phase and G2/M phase of the cell cycle was significantly increased in the ONFH group. Conclusion: Thus, CFA combined with MPS for 7 weeks can be used to establish an early-stage femoral head necrosis model in rabbits.

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